HIT, IF, HIIT and body fat

I have been a proponent of High Intensity Interval Training (HIIT), Intermittent Fasting (IF), and High Intensity Training (HIT) as methods to improve my body composition.

I’m seemingly reading an article every week about the benefits of Tabata training, or HIIT, especially when checking out the tweets of @HealthHabits. Here are a few links that I have ran across:

You Don’t Know HIIT

HIIT is your best choice for burning off Belly Fat

10 more reasons to love High Intensity Interval Training

HIIT v.s. Type 2 Diabetes

Take a look at the laundry list of benefits from the 10 reasons post by Health Habits:

1. HIIT was better than the standard  multidisciplinary approach (exercise, diet and psychological support) at helping overweight kids reduce their cardiovascular risk factors.  Here’s the study
2. HIIT can prevent cardiac death in type 2 diabetic individuals. Here’s the study
3. HIIT should be a required treatment for all Metabolic Syndrome patients. 16 weeks of HIIT training significantly reduced their risk of cardiovascular disease, in terms of improved VO2max, endothelial function, blood pressure, insulin signaling, and plasma lipid composition. Here’s the study
4. HIIT substantially improves insulin action. Say bye-bye to type 2 diabetes & metabolic syndrome. Here’s the study
5. HIIT increases levels of HDL cholesterol – that’s the  good cholesterol. Here’s the study
6. HIIT improves the HRR (Heart Rate Recovery – a measure of how quickly your heart returns to normal post-exercise)) in already well-trained cyclists. Here’s the study
7. HIIT drastically improves cardiovascular function (V02max) in patients with COPD (Chronic Obstructive Pulmonary Disease) Here’s the study
8. Interval training produced a 302% greater increase inV02max when compared to a long, slow distance training protocol. Here’s the study
9. HIIT significantly improved the aerobic fitness of a group of prepubescent children (aerobic fitness measured by peak oxygen consumption  Here’s the study
10. HIIT improves the erectile function of hypertension patients  Here’s the study fellas

What’s not to like?

Moving on to Intermittent Fasting (IF), Martin Berkhan has an informative site, Leangains, where much of the success of his program he attributes to IF.

Here are a few of his posts on IF:

Intermittent Fasting For Weight Loss Preserves Muscle Mass?

Fasted Training Boosts Muscle Growth?

Brief Summary of Popular Approaches to Intermittent Fasting

Dr. Eades also wrote a two part post on Tim Ferriss’ blog:

Real Life Extension: Caloric Restriction or Intermittent Fasting (Part 1)

Real Life Extension: Caloric Restriction or Intermittent Fasting (Part 2)

From Eades in Part 1:

Intermittent fasting (IF) reduced oxidative stress, made the animals more resistant to acute stress in general, reduced blood pressure, reduced blood sugar, improved insulin sensitivity, reduced the incidence of cancer, diabetes, and heart disease, and improved cognitive ability. But IF did even more. Animals that were intermittently fasted greatly increased the amount of brain-derived neurotrophic factor (BDNF) relative to CR animals. CR animals don’t produce much more BDNF than do ad libitum fed animals.

Eades concludes in Part 2:

It’s looking like the intermittent fast is another of those ideas in science that looks good in animal studies then not so good in human studies, proving once again that rats and mice aren’t simply furry little humans. And it appears – for humans, at least – that the intermittent fast is indeed beginning to look like the reality of a late-night gimmicky infomercial: long on promises, short on delivery. I suspect that it is also a cautionary tale about the applicability of caloric restriction studies to humans.

Sorry to be the bearer of bad news, but that’s the way science sometimes works. Lab results and reality are often two different animals.

Then there is Body by Science (by Doug McGuff), Slow Burn Training (by Fred Hahn), and High Intensity Training (The HIT FAQ has been around for quite a while) and you could argue that HIT can trace its origins back to the 6th century BC and Milo of Croton:

Legends say he carried his own bronze statue to its place at Olympia, and once carried a four-year-old bull on his shoulders before slaughtering, roasting, and devouring it in one day. He was said to have achieved the feat of lifting the bull by starting in childhood, lifting and carrying a newborn calf and repeating the feat daily as it grew to maturity. (Wikipedia)

Milo was using the principles of progressive overload training, which is essentially the foundation of any HIT program. You need to put the muscle under enough load that it induces a compensatory response that ultimately builds more muscle.

If you read Body by Science, the author claims that you can achieve the following in 12 minutes a week:

• Build muscle size and strength
• Optimize cardiovascular health
• Ramp up your metabolism
• Lower cholesterol
• Increase insulin sensitivity
• Improve flexibility
• Manage arthritis and chronic back pain
• Build bone density
• Reduce your risk for diabetes, cancer, heart attack, and more

I don’t think it would be a misrepresentation to say Slow Burn Training with Fred Hahn seems to incorporate many of the same principles as Body by Science with Doug McGuff. Mr. Hahn included Body By Science and a book by Matt Bryzcki - who had a big hand in the HIT FAQ - in his top ten strength training books.

Admittedly, I tend to gravitate toward these things because of the purported changes they can induce in the interior milieu.

You are not what you eat, you are what you do with what you eat.

With exercise, it’s not so much about what we do or how much we do it, it’s about how our body responds to the stimulus it is given that we should care about.

So I was listening to a podcast by Jimmy Moore called Low Carb Conversations (you down with LCC?) with Tom Naughton as a guest, who started talking about advice given to people who are going through a weight loss stall while dieting or on a low-carb diet.

Tom had some great points to make (paraphrasing a bit):

Naughton: You become fat for a biochemical reason. And right now, you are as fat as you biologically need to be.

Because of the hormone balance [or imbalance, short-term leading to long-term], you are as fat as you need to be to allow the body to supply itself with fatty acids.

You can continue doing things with your diet, maybe with some HIIT, [or HIT] maybe with IF, but all those things are going to accomplish is to change your biochemistry in such a way that your body is willing to live with less body fat.

When I thought about what Tom was saying, I thought about it in this context: even engaging in HIT, HIIT, and IF is trying to consciously manage our weight, so long as we essentially have to keep these things up in perpetuity in order for them to have lasting effect.

They induce internal changes, but they are fleeting if we don’t continue to get to the weight room and overload our muscles, or sprint in between telephone poles for the rest of our lives. Perhaps our ancestors didn’t have “conscious control” over these behaviors; maybe they had to run from a predator or two, or chase down their dinner, and they had to ‘lift things up and put them down’ out of necessity, but having to rely less on these forms of movement and eating patterns most likely has next to nothing to do with why we get fat as a species.

The key is almost assuredly diet - and you could argue that we need to consciously control what we put into our shopping carts in modern times - however, after this decision is made and we choose to eat only protein and fat from unadulterated, naturally-occurring animals for example, our weight should settle to a relatively healthy level (if we have no underlying metabolic, hormonal, enzymatic, etc. damage) unconsciously.

We don't need to consciously eat more or less. We don't need to consciously move more or less. The quality of the food will dictate our normality. Not quantity. Quantity is a side-effect of quality. We eat less and move more because we're getting leaner, not the other way around.

As you move farther back in time, it becomes progressively more difficult to make the argument that we had conscious control over what we ate. We ate what was available, and while this doesn't imply that whatever was available was necessarily good for us, it does suggest that if the overwhelming majority of the population did not get fat and sick, the quality of the diet probably played the starring role in the health of most societies.

Animals in the wild don't seem to become chronically fat until they eat food they are not accustomed to and almost assuredly not well-adapted to eat. There was a recent article discussing captive gorillas succumbing to human diseases of civilization, notably obesity and heart disease. What happened when the gorillas were taken off of their captive diet of “high vitamin, high sugar, and high starch foods to make sure they got all their nutrients.” Can you say iatrogenic? What happens when you provide an environment for gorillas in which they can only access the foods they presumably could in the wild?

Going back to this natural diet has changed gorilla behavior. Before, gorillas only ate during a quarter of their day because the food was so packed with nutrients. Now at Cleveland, they spend 50-60 percent of their day eating which is the same amount as in the wild. With all this extra eating, the gorillas have doubled their caloric intake, yet at the same time have dropped 65 pounds each. This brings their weight more in line with their wild relatives.

Getting back to HIIT, HIT, and IF, it's not likely that these were the determining factors for preventing or acquiring obesity and western disease if they needed to be under our conscious control. They still may be useful, where you could make the argument that sprinting every once in a while, walking often, missing a few meals here and there are a big part of our history and part of what makes us human. This is Sissonian philosophy at its finest and it’s probably not a bad idea to emulate this.

Now back to Mr. Naughton:

Naughton: All of us are going to hit a certain level of body fat that our bodies do not want to drop below. If that happens to be 20% body fat and you just can't get below it, then focus on the improvements that you've already made, focus on how much better you feel, but understand that depending upon how much metabolic damage you've already done, you may never get to the level of leanness that you had when you were 20. It just might not happen.

As I’ve heard Gary Taubes say: a restricted-carbohydrate diet will help you get to
the leanest you can naturally be, but the leanest you can be may not necessarily be lean.

I want to point out that it's not necessarily phrased in the right context that your body doesn't want you to be leaner than 20%, where the implication is that we seem to be fighting our bodies (and when people invoke 'set point,' the implication is that we're fighting our brain), rather this is where our body fat "settles" at when we have our ducks in a row to the best of our ability, i.e., a good diet, HIIT, HIT, and IF and it settles where it settles. We most likely have a settling point, not a set point.

The way our settling point would lower is to help remove whatever is damming up the system. Might be that insulin is overly secreted and we can't get it in check with
conventional means, or that we’re resistant to insulin, or it could be another factor or force within that is contributing to the lake overflowing, or in the case of humans, over-sized and/or over-numbered, fat cells.

This is what many people in the CrossFit community, and the bodybuilding community come to grips with when they may settle at 14% body fat, and then they train regularly and settle around 10% (so long as they continue their regimen) and then they come to guys like me, but more often and recognizably to someone like Robb Wolf and say "how
do I lean-out?" and the morbidly obese person might overhear the conversation and will think this person must be on drugs or has an eating disorder. They might be right.

Now the 10% dude starts focusing on getting more sleep, getting more sunshine, doing heavier lifting and lower intensity workouts and restricting calories and their body fat may settle around 6%.

So they remain at 6%, and their body fat settles at this level, which means the competition of forces leads to a fat mass that comprises 6% of this person's total body weight. They are dispensing every conscious and unconscious weapon they can think of to try and keep their fat mass down. 

It’s as if he’s bailing out a leak in a boat and he has found a strategy where he can stay afloat (in this case 6% body fat is his buoyancy) as long as he keeps churning.

But once some of the forces are removed, for example, no more weight lifting sessions, the fat may settle at a different level. And say he decides to start drinking 3 Big Gulps a day along with a cavalcade of sugar and refined-carbohydrate-laden foods, and he becomes hyperinsulinemic. This is an added force on the system and is likely to change where his fat mass settles.

With IF as a strategy for weight loss, it may not be a stretch that it is similar to caloric restriction (CR) in that both will have to be theoretically implemented for life in order to maintain the change induced by the strategy.

But the same can be said of a low-carb or Paleo diet; these things need to be maintained in order to maintain the effects they are having on (and in) the body. In the modern world, we need to consciously avoid carbohydrates at every turn if we're on a low-carbohydrate diet and we have to avoid about 85% of the offerings in a typical grocery store if we're eating Paleo (or low-carb). The percentage of food that we shouldn't be eating in a grocery store might be the same number as the prevalence of obesity (last time I checked it was hovering around 70%). But if we can navigate past the soda, sweets, and snacks aisle, and fuel our bodies with the appropriate foods, consciousness has nothing to do with why we get fat.

This also makes any recommendation to go on a low-carb diet for weight loss, and then once you reach a desirable weight, go ahead and revert back to the Standard American Diet (SAD) - but be sure to practice calorie balance! - patently absurd.

Every Tom, Dick, and Harry can tell his office colleagues or park bench neighbors the latest on reducing diets.  More than in any other illness, the physician is called upon only to do a special trick, to make the patient do something—stop eating—after it has already been proved that he cannot do it. -Hilde Bruch, The Importance of Overweight

And one distinction that should be made between IF and CR is that many of the purported benefits of IF are not from a reduction in calories, whereas CR implies that you are going to have to go starving on some level for the rest of your life to maintain the benefits of CR.

Even those people who are properly informed and anxious to exercise voluntary control, frequently fail in the prevention of overweight.  Evidently, it is not an easy matter continuously to overrule persistent impulses. Unfortunately we cannot in most cases correct these impulses by attacking their source, namely, the anomaly of the regulatory mechanism; and so long as man has to rely on his will power to suppress persistent impulses, prevention of obesity will remain a relatively rare accomplishment. -Hugo Rony, Obesity and Leanness

Saturated and Fat and Heart Disease

Most people think that it’s saturated fat that can lead to elevated levels of cholesterol (specifically, LDL), and because our cholesterol goes up, we will be at an increased risk of heart disease and death.

Here is a 40-second advertisement from the UK Government regarding saturated fat:





Interesting to note (and Tom Naughton did as well in Big Fat Fiasco) that apparently saturated fat is a liquid in the refrigerator and solid at room temperature. And if you follow the logic that anything that clogs your drain-pipe will clog your arteries, probably leaves you with just H2O to consume.

The incidence of heart disease is not decreasing, yet we’re eating less saturated fat.

Also, invoking the logic that saturated fat raises cholesterol; and high cholesterol clogs your arteries; and clogged arteries cause heart disease; therefore a diet high in saturated fat causes heart disease is a logical fallacy (and one could argue that each link in this chain is unsubstantiated as well).

Drinking excess water leads to frequent urination. Frequent urination is linked to diabetes. Therefore, drinking too much water will give you diabetes.

There is an increase in sales of ice cream in the summer. There is a higher incidence of drowning in the summer. Ice cream leads to drowning.

There is an increase in the number of observed umbrellas outside when it’s raining. Umbrellas cause rain? No. They’re at the scene of the crime, but not necessarily the culprit.

A clinical trial in the 1970s tested the effects of a cholesterol-lowering drug called clofibrate, which lowered cholesterol in subjects. The trial had to be stopped because the men taking the pill had a 47% higher death rate than the placebo group. [1]

By the same logic invoked above, I can say that a low-fat diet reduces cholesterol, and lower cholesterol (via clofibrate) led to more deaths, therefore low-fat diets kill you.

Virtually every trial that tried to support the fat/heart disease connection has failed. What do good scientists do when faced with overwhelming contradictory evidence? They admit their hypothesis failed and they explore other questions.

If you replace saturated fat in your diet with cereal, skim milk, a banana and an orange, your LDL may go down, but your triglycerides will go up. Your HDL will go down. And now you’re at a higher risk of heart disease. These are better predictors than LDL, but they, too, have their limitations.

Also, More saturated fat does not mean less HDL, as many people seem to believe. In a meta-analysis of 27 studies on serum lipids (Mensink and Katan, 1992), the study noted: “All fatty acids elevated HDL cholesterol when substituted for carbohydrates, but the effect diminished with increasing unsaturation of the fatty acids.”

In other words, if the diet was rich in saturated fats, it would increased HDL, and if you replace the saturated fats with unsaturated fats (or synthetic trans fats), your HDL is likely to decrease.

In a 2010 meta-analysis of prospective cohort studies evaluating the association between saturated fat with cardiovascular disease,  the authors, Siri-Tarino, Sun, Hu, and Ronald Krauss stated: “there is no significant evidence for concluding that dietary saturated fat is associated with an increased risk of CHD or CVD.”

In another article by the same authors: “An independent association of saturated fat intake with CVD risk has not been consistently shown in prospective epidemiologic studies, although some have provided evidence of an increased risk in young individuals and in women. Replacement of saturated fat by polyunsaturated or monounsaturated fat lowers both LDL and HDL cholesterol.”

Another study from 2010 (Yamagishi et al.) entitled “Dietary intake of saturated fatty acids and mortality from cardiovascular disease in Japanese,“ found that people who ate the most sturated fat had a lower risk of cardiovascular disease and the authors stated, keeping in mind that stroke is a bigger public health threat than heart disease in Japan: “SFA intake was inversely associated with mortality from total stroke, including intraparenchymal hemorrhage and ischemic stroke subtypes, in this Japanese cohort.”

But can the associative studies be reconciled with experimentation and mechanisms of action? [2]

The Siri-Tarino (2010) article continued: “replacement of saturated fat by polyunsaturated or monounsaturated fat lowers both LDL and HDL cholesterol. However, replacement with a higher carbohydrate intake, particularly refined carbohydrate, can exacerbate the atherogenic dyslipidemia associated with insulin resistance and obesity that includes increased triglycerides, small LDL particles, and reduced HDL cholesterol. In summary, although substitution of dietary polyunsaturated fat for saturated fat has been shown to lower CVD risk, there are few epidemiologic or clinical trial data to support a benefit of replacing saturated fat with carbohydrate. Furthermore, particularly given the differential effects of dietary saturated fats and carbohydrates on concentrations of larger and smaller LDL particles, respectively, dietary efforts to improve the increasing burden of CVD risk associated with atherogenic dyslipidemia should primarily emphasize the limitation of refined carbohydrate intakes and a reduction in excess adiposity.”

In other words, it’s the carbohydrates, not the dietary fats that are contributing to CVD risk associated with atherogenic lipid dysreguation.

After we eat a meal with a lot of sugar and/or carbohydrates, the bloodstream gets flooded with glucose, and the liver takes some of the glucose and converts it into triglycerides for storage. The triglycerides are fused to the apo B protein and to the cholesterol that forms.

Gary Taubes wrote in Good Calories, Bad Calories (2007):

The triglycerides constitute the cargo that the lipo-proteins drop off at tissues throughout the body. The combination of cholesterol and apo B is the delivery vehicle.  The resulting lipoprotein has a very low density, and so is a VLDL particle, because the triglycerides are lighter than either the cholesterol or the apo B.  (In the same way, the more air in the hold of a ship, the less dense the ship and the higher it floats in the water.)  For this reason, the larger the initial oil droplet, the more triglycerides packaged in the lipoprotein, the lower its density.

The liver then secretes this triglyceride-rich VLDL into the blood, and the VLDL sets about delivering its cargo of triglycerides around the body.  Throughout the process, known poetically as the delipidation cascade, the lipoprotein gets progressively smaller and denser until it ends its life as a low-density lipoprotein—LDL.  One result is that any factor that enhances the synthesis of VLDL will subsequently increase the number of LDL particles as well.  As long as sufficient triglycerides remain in the lipoprotein to be deposited in the tissues, this evolution to progressively smaller and denser LDL continues.  It’s this journey from VLDL to LDL that explains why most men who have high LDL cholesterol will also have elevated VLDL triglycerides.  “It’s the overproduction of VLDL and apo B that is the most common cause of high LDL in our society,” says Ernst Schaefer, director of the lipid-metabolism laboratory at the Jean Mayer USDA Human Nutrition Research Center on Aging at Tufts University.  None of this, so far, is controversial; the details are described in recent editions of biochemistry textbooks.

How this process is regulated is less well established.  In Krauss’s model, based on his own research and that of the Scottish lipid-metabolism researcher Chris Packard and others, the rate at which triglycerides accumulate in the liver controls the size of the oil droplet loaded onto the lipoprotein, and which of two pathways the lipoprotein then follows.  If triglycerides are hard to come by, as would be the case with diets low in either calories or carbohydrates, then the oil droplets packaged with apo B and cholesterol will be small ones.  The ensuing lipoproteins secreted by the liver will be of a subspecies known as intermediate-density lipoproteins—which are less dense than LDL but denser than VLDL—and these will end their lives as relatively large, fluffy LDL.  The resulting risk of heart disease will be relatively low, because the liver had few triglycerides to dispose of initially.

If the liver has to dispose of copious triglycerides, then the oil droplets are large, and the resulting lipoproteins put into the circulation will be triglyceride-rich and very low-density.  These then progressively give up their triglycerides, eventually ending up, after a particularly extended life in the circulation, as the atherogenic small, dense LDL.  This triglyceride-rich scenario would take place whenever carbohydrates are consumed in abundance.  “I am now convinced it is the carbohydrate inducing this atherogenic [profile] in a reasonable percentage of the population,” says Krauss.  “. . . we see a quite striking benefit of carbohydrate restriction.”

Low-Carbohydrate Studies: Part IV

Previous related posts:

Part I | Part II | Part III

“It would not perhaps be too fanciful to say that a new idea is the most quickly acting antigen known to science.  If we watch ourselves honestly we shall often find that we have begun to argue against a new idea even before it has been completely stated.” –Wilfred Trotter, cited in W.I.B. Beveridge, The Art of Scientific Investigation, 1950.

Weight Loss and Macronutrient Composition

The carbohydrate hypothesis is not a new idea - it has been invoked in one way or another for at least 185 years (23), but it is perceived as a new phenomenon, or "fad," by the researchers conducting diet studies as well as the public health authorities, and they have argued against the hypothesis before it has been completely stated and properly explained.

The unrelenting argument made by proponents of the positive-calorie hypothesis is that the only thing that matters in terms of weight loss, weight gain, or weight maintenance is balancing calorie intake with calorie expenditure.  There is nothing special about different proportions of carbohydrates, fats, and protein when it comes to weight control, it’s all about energy in versus energy out, 'a calorie is a calorie is a calorie,' say the researchers in diet studies. (They might, on the other hand, tell you that too much dietary fat will cause heart disease, so eat a low-fat diet, but that’s another story.)

When weight loss turns out to be greater on a low-carbohydrate diet compared to a low-fat diet, which is often the case, the authors will make note that the reason why the low-carb dieters lost more weight was because they consumed less calories.

What escapes the researchers, who are supposedly testing the carbohydrate hypothesis – that it’s the carbohydrates that make us fat, not the fat and protein – is the question as to why the low-carb group which is unrestricted in calories would consume less than a low-fat group of dieters who are restricted in calories?

Also, if the researchers could suspend their calories-in/calories-out hypothesis belief for just a few more moments, and apply the carbohydrate hypothesis, perhaps the weight loss observed on the low-fat, calorie-restricted diets, too, stem from the reduction in carbohydrates from baseline.  That is, when subjects go on a clinical low-fat diet, they are not only eating less fat, they’re eating less of everything, because they are also restricted in calories.  These people are not only eating less dietary fat than before their diet began, but they’re also eating less carbohydrates.

In a 2010 study by Foster et al. in the Annals of Internal Medicine (1), the authors also noted that the similar weight losses observed with low-carbohydrate and low-fat diets in their study demonstrated that the comprehensive lifestyle intervention produced the same energy deficit in both groups, despite marked differences in their behavioral targets.

However, there are a number of possibilities as to why weight loss was the same in both groups.  As previously discussed, the low-carbohydrate group were increasing their carbohydrate consumption until a “stable and desired weight was achieved.”  It’s possible that by the end of the study, both groups were eating a similar diet in terms of nutrient composition.

Also, as noted above, the authors added another variable to the study: "Both diets were combined with behavioral treatment."  This is an admitted limitation of the study by the researchers, and makes it impossible to discern whether the behavioral modification alone was responsible for the weight loss in both groups, whether the low-carbohydrate diet and low-fat, low-calorie diets played the predominant role in weight loss, or whether it was a combination of behavioral modification and the diets (or increased expenditure, as the subjects were instructed to participate in 200 minutes of aerobic exercise per week).  The inclusion of a behavioral treatment in a diet study testing the effectiveness of two different diets invalidates the proposed hypothesis.  This should be covered in greater detail in a separate blog post.

The authors (1) concluded that the long-term findings in an outpatient setting in which there were not significant differences in weight was consistent with data from short-term metabolic ward studies (2-4) showing that macronutrient composition did not influence weight loss when energy content was fixed.

Trials from short-term metabolic wards are particularly illuminating since these types of studies usually have the ability to control a number of variables that under non-metabolic ward conditions are otherwise uncontrolled.  Investigators can carefully measure the food to be administered to the subjects and monitor the amount and type of food eaten.  To be sure, metabolic ward studies are not without limitation, but they can generally close a number of the loopholes that arise in outpatient settings.  

Self-reporting nutrient intake is one of the biggest limitations to most diet studies, and this was the supposed reason why Foster et al. (1) did not collect any nutrient intake data from their subjects.

In other words, with inpatient metabolic wards studies, as compared to the Foster et al. (1) study, the researchers fed the subjects the food they were supposed to eat; the researchers monitored how much food the subjects ate, the researchers collected the data on food intake; the researchers analyzed the data on how much food the subjects were eating; and the researchers reported how much food their subjects actually ate rather than: not feeding, monitoring, collecting, analyzing, nor reporting the amount and type of food their subjects were eating, and estimating how much food the subjects that dropped out of the study ate and how much weight they might have lost had they stuck around (this is called ‘Intention to Treat Analysis, or ITT, and should be discussed in detail in a later post), which is what the researchers did in Foster et al. (1) as well as many other randomized trials of low-carbohydrate diets compared to low-fat, calorie-restricted diets (5-10).

Whether a diet study with no recording or reporting of intake is more limited than a study with self-reporting may be open for debate, however, a study comparing two different diets with no data on what their subjects actually ate is invalid in terms of making conclusions about the effects of such diets in the trial.

The metabolic ward studies cited in the Foster et al. (1) paper were:

Yang and Van Itallie, 1976 (2): 800 kcal diets (isocaloric)

Golay et al, 1996 (3): 1000 kcal diets (isocaloric)

Boden et al, 2005 (4): (“usual diet,” followed by a low-carbohydrate diet)

In Yang and Van Itallie (2), intake for the "mixed" diet contained 90 g/d of carbohydrates, where the typical recommendations of 55-65% carbohydrates based on a 2000-calorie diet amounts to as much as 325 g/d of dietary carbohydrates.  This is a potential 72% reduction in the carbohydrate content of the diet of a diet that is supposedly liberal in carbohydrates, if we presume subjects were eating something close to a mixed diet prior to the study.  If we had an idea what the low-carbohydrate diet subjects in Foster et al. (1) were consuming at 24 months, it may have been instructive.  It would be likely that the low-carbohydrate group were consuming more than 90 g/d of carbohydrates by the end of the study, which means that they would have been eating more carbohydrates on a “low-carbohydrate” diet than a “mixed diet.”

To wit, in Gardner et al. (6), a one-year randomized trial among 311 overweight/obese (body mass index, 27-40), nondiabetic premenopausal women, "Participants were randomly assigned to follow the Atkins, Zone, LEARN, or Ornish diets and received weekly instruction for 2 months, then an additional 10-month follow-up."

In the Atkins group, after 2 months, subjects reported an average intake of 1381 calories, with 17.7% derived from carbohydrates, which amounts to approximately 61 g/d.

After 6 months, subjects reported an average intake of 1538 calories, with 29.5% derived from carbohydrates, which amounts to approximately 113 g/d.

After 12 months, subjects reported an average intake of 1599 calories, with 34.5% derived from carbohydrates, which amounts to approximately 138 g/d.

It’s important to note that the nutrient intake data was collected via self-reporting, which can be unreliable, however it does provide trends in dietary patterns in which we can glean some potentially useful information. The Gardner et al. (6) study helps illustrate the point that for most of the trial, subjects were reportedly eating more carbohydrates than the low-fat, isocaloric (or "mixed") diets from the metabolic ward studies (2, 3).

A significant limitation in regard to the nutrient composition of the diet with the Yang and Van Itallie (2) study is the low caloric content of the diet for both groups, which makes the "mixed" diet a "low-carbohydrate diet," or at least lower than subjects trying to adhere to a low-carbohydrate diet.


Golay et al. (3) had the same limitation.  Subjects were assigned to either a 15% carbohydrate diet or a 45% carbohydrate diet.  The 45% carbohydrate diet consisted of an average of 115 g/d carbohydrates, an amount below the Atkins subjects from Gardner et al. (6) after 12 months (138 g/d).

 

For the sake of argument, take an example of a metabolic ward study conducted on two individuals, both eating 10 calories per day for two weeks.

One individual is assigned to a low-fat diet. The subject is fed a diet that is 60% of calories from carbohydrate, 25% fat, and 15% protein.

The other individual is assigned to a low-carbohydrate diet: 20% of calories from carbohydrate, 65% fat, and 15% protein.

If there was no difference in weight loss between the two subjects (i.e., both individuals lost 5 kg), would the authors conclude that the results were consistent with metabolic ward studies showing that macronutrient composition did not influence weight loss when energy content was fixed?

Would they comment on whether in fact these individuals may have been starving on both diets and that individuals severely restricting their intake of nutrients may be fundamentally different from patients who are allowed diets unrestricted in calories?

Also, if the researchers are testing the carbohydrate hypothesis, this type of study would not refute it because in both groups, carbohydrate consumption would be considered very low (1.5 g/d of carbohydrates in the low-fat group  and 0.5 g/d of carbohydrates in the low-carbohydrate group per day) and both were effective for weight loss.

In the third metabolic ward study referenced by Foster et al. (1), Boden et al. (4) was an inpatient comparison of two diets on the same 10 individuals (obese patients with type 2 diabetes), beginning with the "usual diet," which consisted of continuing their usual diet for 7 days, followed by a 14-day ad libitum, low-carbohydrate diet.  From the abstract:

“On the low-carbohydrate diet, mean energy intake decreased from 3111 kcal/d to 2164 kcal/d. The mean energy deficit of 1027 kcal/d (median, 737 kcal/d) completely accounted for the weight loss of 1.65 kg in 14 days (median, 1.34 kg in 14 days).”

Doesn’t this beg the question:  why would the subjects voluntarily reduce their intake from their “usual diets” by over 1000 calories when they went on a “low-carbohydrate diet” for two weeks?

Also, note the Atkins diet was ad libitum in the Gardner et al. (6) study and subjects reportedly consumed just 1381 calories, well below their baseline of 1888 calories.  The relevant question is whether there is a relationship between the carbohydrate content of the diet and caloric consumption, and claiming that ‘macronutrient composition did not influence weight loss when energy content was fixed’ does not answer it.

The authors in Boden et al. (4) stated: 

"In a small group of obese patients with type 2 diabetes, a low-carbohydrate diet followed for 2 weeks resulted in spontaneous reduction in energy intake to a level appropriate to their height; weight loss that was completely accounted for by reduced caloric intake; much improved 24-hour blood glucose profiles, insulin sensitivity, and hemoglobin A1c; and decreased plasma triglyceride and cholesterol levels. The long-term effects of this diet, however, remain uncertain."

It should be highlighted that the authors concluded that the low-carbohydrate diet resulted in “spontaneous reduction in energy intake to a level appropriate to their height” and that “weight loss was completely accounted for by reduced caloric intake.”

Again, the authors need to address the phenomenon of subjects voluntarily reducing their caloric intake when “patients could eat protein and fat as much and as often as they wanted,” including “beef patties, ground turkey patties, chicken breasts, turkey slices, fresh ham slices, raw or steamed vegetables, butter, and diet gelatin,” and “as with their usual diets, participants could request allowable items that were not available from the hospital kitchen, such as fresh fish, eggs, various cuts of beef, cream, and additional vegetables,” as well as “limited amounts of cheese and cream cheese,” in addition to “specific brands of salad dressings and snack foods suggested by Dr. Atkins, including Atkins-brand foods (4).”

During the first week of the study, on the usual diet, patients maintained their usual eating and activity patterns, and the authors concluded “mean caloric intakes and total energy expenditures were in balance (approximately 3100 kcal/d) and body weights remained stable."

The authors stated that because all weight loss was due to loss of fat, and they estimated that the caloric deficit plus changes in body water accounted for all weight loss, they concluded that their data did not support the concept that the weight loss induced by the low-carbohydrate diet was due to different metabolic utilization of macronutrients (12, 13).

The researchers admittedly had no explanation for why the subjects spontaneously reduced their appetite (4). The authors in Boden et al. (4) noted that lack of variety and palatability have been incriminated, but were not supported by their reports from subjects via visual analogue scale questionnaires.

It’s also not supported by observational accounts. Journey over to Dr. Michael Eades’s blog for a tale of two diet studies, which illuminates some of these accounts and compares the Minnesota starvation study by Ancel Keys to a low-carbohydrate study by John Yudkin (14). This blog post further discusses the fact that low-carbohydrate dieters voluntarily reduce their caloric consumption to levels that Keys subjected his subjects to in order to induce starvation in a relatively high-carbohydrate diet.

The authors in Boden et al. (4) postulated that decreased serum insulin levels observed in their subjects on a low-carbohydrate diet may have reduced appetite because studies in humans have found that insulin increased food intake (15-17).

Also, the authors found mean plasma leptin levels were lower, and thought this may have to do with caloric restriction (18, 19) and decreased insulin levels (20) or because leptin sensitivity had increased. They concluded that in view of the appetite-suppressing effect of leptin (21), lower leptin levels may have stimulated appetite and limited diet-induced weight loss.

It seems odd to state that there is no metabolic advantage to a low-carbohydrate diet and that macronutrient composition makes no difference in terms of weight regulation, when, if their hypotheses above are true, wouldn’t it be an advantage that when insulin levels are low, more stored fat is mobilized? However, according to the logic of Boden et al. (4), if the low-carbohydrate dieters are mobilizing more stored fat, and thus they require less calories than someone on a low-fat diet who is mobilizing less, it's somehow irrelevant to the conversation of weight gain and it’s still the calories that matter.

Note that the authors in Boden et al. (4) are addressing the question of why their subjects reduced their caloric intake volitionally on a low-carbohydrate diet unrestricted in calories, which is a discussion that most of the journal articles comparing low-carbohydrate, ad libitum and low-fat, calorie-restricted diets omit. So kudos.

The statement regarding decreased insulin levels reducing appetite and lower leptin levels stimulating appetite is contradictory.  On one hand, the investigators are trying to make the case for why the patients reduced their caloric intake by a reduction in appetite (3111 kcal/d to 2164 kcal/d, a 30% voluntary reduction in energy intake), yet conversely argue that the lower leptin levels may have increased their appetite.

If their appetite was increased, why were they eating 1000 fewer calories than their usual diet?  Are the authors arguing that if leptin levels remained the same, they would have further reduced their caloric intake?  It’s entirely possible, but the authors are probably closer to the truth by reasoning that perhaps leptin sensitivity had increased.  More leptin may be detected because more fat is mobilized (via lower levels of insulin) with a restricted-carbohydrate diet.

Also, insulin is the primary regulator of fat storage and is the “gatekeeper” for fat mobilization and storage.  This is isn't controversial from a biochemical standpoint. When insulin levels are elevated, fat storage is promoted and fat mobilization inhibited.  Conversely, when insulin levels are low, fat mobilization is promoted and fat storage inhibited.  That carbohydrates drive insulin secretion, and insulin promotes fat deposition is central to the carbohydrate hypothesis.  In this scenario, an increase in caloric intake and/or a decrease in energy expenditure are side effects of eating a diet high in sugar and easily digestible carbohydrates.

In Boden et al. (4), the low insulin levels of the subjects meant that they had relatively more access to their stored adipose tissue relative to when they were on their “usual” diet.  If more free fatty acids are available for use, it is conceivable that they would need less exogenous fuel and their energy intake requirements would decrease (to the possible tune of a 30% reduction, as witnessed in the study). The “dieters” are eating their own adipose tissue. In this context, the voluntary decrease of 1000 kcals makes more sense: there’s no caloric deficit per se, rather the Atkins subjects are supplementing their exogenous fuel with endogenous sources (liberated fatty acids from adipose tissue).

Ultimately, while the authors address the question of why their patients reduced caloric intake, they didn’t have any answer, as was noted in the paper.

Likewise, it is not a sufficient explanation by Foster et al. (1) to conclude that macronutrient composition does not affect weight loss by citing three metabolic ward studies; two in which the researchers were ostensibly comparing low-carbohydrate diets to very low-carbohydrate diets (2, 3), and a third study that observed a voluntary reduction in 1000 calories from their usual diet (4).

Even if you are a proponent of the calories-in/calories-out hypothesis, if lowering carbohydrates seems to induce lower caloric consumption, while lowering fat doesn’t have the same effect, wouldn’t you entertain the notion that macronutrient composition does in fact influence weight loss, and the decreased caloric consumption seen on a low-carbohydrate diet may be a consequence of the restricted-carbohydrates in the diet?  And the caveat that macronutrient composition does not influence weight loss when energy content is fixed only seems to be applicable if we are starving our subjects.

In light of this, a good test of the competing calories-in/calories-out and carbohydrate hypotheses would be an isocaloric metabolic ward study in which the groups were not starved, or semi-starved, rather the two groups are fed high-calorie diets with different macronutrient composition.  This would eliminate the fact that when subjects are treated to semi-starvation diets of different macronutrient compositions, they’re invariably eating fewer carbohydrates than they were before the intervention, even if they're placed in the low-fat-diet group.

In a study by Shai et al. (24) for example, the low-fat dieters reduced their carbohydrate consumption by 83 g/d from baseline after 24-months on the diet in a 24-month study.  The low-fat diet group in Gardner et al. (6) (LEARN) reportedly reduced their carbohydrate consumption by 37 g/d after 12-months in a 12-month study. Perhaps the reported weight loss on these diets is also due to the restricted nature of the carbohydrates, and perhaps the improvement of the quality of the carbohydrates on such diets (which will be discussed in more detail later)?

A good place to start (and for me to end this post) in the search for a true test of the carbohydrate hypothesis is the type of trial that Gary Taubes proposed in the afterword of Good Calories, Bad Calories (22):

[T]here are indeed relatively simple experiments that could establish whether it’s excess calories that make us fat (the conventional wisdom) or purely the effect of carbohydrates on insulin and insulin on fat accumulation (the carbohydrate hypothesis).

Such experiments could be done with a dozen subjects in to two to three months and so would be inexpensive, at least by the standards of modern medical research.  One caveat is that they would require that their human subjects be treated to some extent like laboratory animals.  They would be housed in a metabolic ward and fed three or more meals a day.  In the ideal situation, the subjects would never leave the ward and be under constant observation—as was the case with Vilhjalmur Stefansson and his colleague Karsten Anderson in the first weeks of their 1928 meat diet experiment—so that the opportunity to cheat on their diets would be minimized.  In one variation of the experiment, the subjects would be randomized into two groups.  One group, the controls, would be fed a balanced diet, relatively rich in carbohydrates, constituting 3,000 or even 4,000 calories a day.  The other would be fed a diet of equal caloric content, but severely carbohydrate restricted—preferably less than sixty grams of carbohydrates a day.

The carbohydrate-restricted diet would lower insulin levels significantly.  According to the carbohydrate hypothesis, this would reduce fat accumulation independent of the calories consumed.  The fatty acids liberated from the fat tissue would be burned as fuel and energy expenditure would increase in these subjects.  The balanced diet would have no effect on insulin levels and those subjects would not be expected to lose weight or increase energy expenditure. (Because even the balanced diet might represent an improvement in the quality of the carbohydrates in the subjects’ diet—calories from sugar, white bread, white rice, and beer, for instance, might be replaced by calories from whole grains and green vegetables—there is always the possibility that even the control group in such a study will lose some weight, even if the amount of calories consumed has no effect.)

The study would have to run for at least two months, long enough to establish a significant amount of fat loss if the carbohydrate hypothesis is correct.  The researchers would measure energy expenditure before the experiment began and then at regular intervals throughout the experiment.  (A technology known as doubly-labeled water would allow this to be done within 10 percent accuracy.)  Insulin levels would also be measured regularly, as would any other blood biomarkers or risk factors for heart disease that the researchers might choose (and be able to afford).  Body composition, before and after the experiment, should be analyzed as well to establish the proportion of lean and fat tissue lost (if any).

Such an experiment would go a long way toward determining the validity of the two competing hypotheses: is it the quantity of calories that determines our weight and fat accumulation or the quality?  I would argue, as I’ve been doing widely since this book came out, that such an experiment is absolutely fundamental to understanding the cause not only of obesity, but of heart disease, cancer, and diabetes, as well.

____________________

1. Foster GD, Wyatt RW, Hill JO, Makris AP, Rosenbaum DL, Brill C, Stein RI, Mohammed BS, Miller B, Rader DJ, Zemel B, Wadden TA, Tenhave T, Newcomb CW, Klein S.  Weight and Metabolic Outcomes After 2 Years on a Low-Carbohydrate Versus Low-Fat Diet.  Ann Intern Med. 2010;153:147-157.

2. Yang MU, Van Itallie TB. Composition of weight lost during short-term weight reduction. Metabolic responses of obese subjects to starvation and lowcalorie ketogenic and nonketogenic diets. J Clin Invest. 1976;58:722-30. [PMID: 956398]

3. Golay A, Allaz AF, Morel Y, de Tonnac N, Tankova S, Reaven G. Similar weight loss with low- or high-carbohydrate diets. Am J Clin Nutr. 1996;63:174-8. [PMID: 8561057]

4. Boden G, Sargrad K, Homko C, Mozzoli M, Stein TP. Effect of a lowcarbohydrate diet on appetite, blood glucose levels, and insulin resistance in obese patients with type 2 diabetes. Ann Intern Med. 2005;142:403-11. [PMID: 15767618]

5. Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, et al. A randomized trial of a low-carbohydrate diet for obesity. N Engl J Med. 2003;348:2082-90. [PMID: 12761365]

6. Samaha FF, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, et al. A low-carbohydrate as compared with a low-fat diet in severe obesity. N Engl J Med. 2003;348:2074-81. [PMID: 12761364]

7. Brehm BJ, Seeley RJ, Daniels SR, D’Alessio DA. A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women. J Clin Endocrinol Metab. 2003;88:1617-23. [PMID: 12679447]

8. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. A lowcarbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Ann Intern Med. 2004;140:769-77. [PMID: 15148063]

9. Stern L, Iqbal N, Seshadri P, Chicano KL, Daily DA, McGrory J, et al. The effects of low-carbohydrate versus conventional weight loss diets in severely obese adults: one-year follow-up of a randomized trial. Ann Intern Med. 2004;140: 778-85. [PMID: 15148064]

10. Dansinger ML, Gleason JA, Griffith JL, Selker HP, Schaefer EJ. Comparison of the Atkins, Ornish, Weight Watchers, and Zone diets for weight loss and heart disease risk reduction: a randomized trial. JAMA. 2005;293:43-53. [PMID: 15632335]

11. Gardner CD, Kiazand A, Alhassan S, Kim S, Stafford RS, Balise RR, et al. Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women: the A TO Z Weight Loss Study: a randomized trial. JAMA. 2007;297:969-77. [PMID: 17341711]

12. Atkins RC. Dr. Atkins’ New Diet Revolution.  New York: Avon Books: 1992.

13. Greene P, Willett W, Devecis J, Skaf A.  Pilot 12-week feeding, weight-loss comparison: low-fat vs. low-carbohydrate (ketogenic) diets (Abstract).  Obes Res. 2003;11:A23.

14. Eades MR. Is a calorie always a calorie? The Blog of Michael R. Eades, M.D. September 11, 2007

15. Rodin J, Wack J, Ferrannini E, DeFronzo RA. Effect of insulin and glucose on feeding behavior. Metabolism. 1985;34:826-31. [PMID: 3897769]

16. Holt SH, Miller JB. Increased insulin responses to ingested foods are associated with lessened satiety. Appetite. 1995;24:43-54. [PMID: 7741535]

17. The effect of intensive treatment of diabetes on the development and progression of long-term complications in insulin-dependent diabetes mellitus. The Diabetes Control and Complications Trial Research Group. N Engl J Med.1993;329:977-86. [PMID: 8366922]

18. Considine RV, Sinha MK, Heiman ML, Kriauciunas A, Stephens TW,
Nyce MR, et al. Serum immunoreactive-leptin concentrations in normal-weight and obese humans. N Engl J Med. 1996;334:292-5. [PMID: 8532024]

19. Boden G, Chen X, Mozzoli M, Ryan I. Effect of fasting on serum leptin in normal human subjects. J Clin Endocrinol Metab. 1996;81:3419-23. [PMID: 8784108]

20. Boden G, Chen X, Kolaczynski JW, Polansky M. Effects of prolonged
hyperinsulinemia on serum leptin in normal human subjects. J Clin Invest. 1997;100:1107-13. [PMID: 9276727]

21. Campfield LA, Smith JF. Central integration of peripheral signals in the regulation of food intake and energy balance: role of leptin and insulin. In: Bray GA, Bouchard C, eds. Handbook of Obesity. 2nd ed. New York: Marcel Dekker;2003:461-79.

22. Taubes G. Good Calories, Bad Calories. Knopf. 2007.

23. Brillat-Savarin JA.  The Physiology of Taste.  1825.

24. Shai I, Schwarzfuchs D, Henkin Y, Shahar DR, Witkow S, Greenberg I, et al; Dietary Intervention Randomized Controlled Trial (DIRECT) Group. Weight loss with a low-carbohydrate, Mediterranean, or low-fat diet. N Engl J Med. 2008;359:229-41. [PMID: 18635428]